Introduction: Cardiac myxoma is a primary benign tumor most often located in the left atrium and it is a rare source of cerebral stroke of young subjects. Case Presentation: We report the case of a young women with cardiac myxoma revelated by hemiplegia. The patient suddenly presented vertigo followed by a fall, a heaviness of her left body, and dysarthria. The brain CT scan and magnetic resonance imaging have revealed cerebral ischemia located in the right Sylvian territory. Transthoracic echocardiography highlighted a round cardiac mass, mobile, heterogeneous, multilobed, appended to the interatrial septum and the atrial side of the large mitral valve by wide implantation and measuring 38x25mm in the parasternal short axis (PSAX) and apical 4 chamber views evocative of left atrium myxoma. After the surgical resection, which was postponed for a month, the removed tumor was sent for histopathological examination. The morphological examination revealed a myxoid tumor proliferation compatible with cardiac myxoma expressing calretinin by these tumor cells in the immunohistochemical study. Conclusions: Left atrium myxoma is a benign cardiac tumor and a rare cause of ischemic stroke. Transthoracic echocardiography facilitates the diagnosis of this tumor which will then be confirmed by histological analysis.

Drugs used to treat cardiovascular disease as well as those used in the treatment of multiple other conditions can occasionally produce exaggerated prolongation of the QT interval on the surface electrocardiogram and the morphologically distinctive polymorphic ventricular tachycardia that results is known as «torsade de pointe». «Torsade de pointe» (TDP) is a characteristic polymorphic ventricular arrhythmia associated with delayed ventricular repolarization as evidenced on the surface electrocardiogram by QT interval prolongation. It typically occurs in self-limiting bursts, causing dizziness and syncope, but may occasionally progress to ventricular fibrillation and sudden death. This rare case report showed the potential higher risk of the occurrences of «Tdp» when levetiracetam (KEPPRA) was used in combination therapy with fluconazole, which is already a known medication with the risk of causing polymorphic ventricular arrhythmia.

Introduction and importance: Laubry–Pezzi syndrome is a rare congenital heart disease characterized by the association of ventricular defect septal to aortic cusp prolapse responsible for aortic regurgitation (AR). Case presentation: We reported three cases of Laubry–Pezzi syndrome diagnosed in our department of cardiology on a cohort of more than 3000 cases of congenital heart disease. A 13-year-old patient presented a Laubry–Pezzi syndrome with severe AR and significant volumetric left ventricle overload and was operated on in time to allow a good evolution of his condition. A 43-year-old patient, followed for congenital cardiac pathology, presented with severe dyspnea. The echocardiogram found global dysfunction of the left ventricle with an ejection fraction of 35%, a perimembranous ventricular septal defect (VSD) almost completely closed by the prolapse of the noncoronary cusp, and severe eccentric aortic insufficiency due to the prolapse of the noncoronary cusp. Aortic valve replacement and VSD closure were indicated. The third patient is a 21-year-old patient with Down syndrome, in whom a grade 2/6 systolic murmur was detected. Transthoracic echocardiography revealed a perimembranous VSD measuring 4 mm without any hemodynamic repercussions and a moderate aortic insufficiency due to the prolapse of the noncoronary cusp. Clinical and echocardiographic monitoring with Osler prevention was indicated as a modality of management. Clinical discussion: The pathophysiology is explained by the Venturi effect, the restrictive shunt of the VSD creates an area of low pressure that sucks the adjacent cusp resulting in aortic prolapse and regurgitation. The diagnosis is essentially based on transthoracic echocardiography; it must be conducted before the emergence of AR. The management of this rare syndrome still remains nonconsensual, whether it is through timing or operative techniques. Conclusion: Management must be early by closing the VSD with or without aortic valve intervention to prevent the onset or worsening of AR.